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姜黄素及其衍生物的屏障保护活性。

Barrier protective activities of curcumin and its derivative.

机构信息

Laboratory of Microvascular Circulation Research, NEUORNEX Inc., Daegu, Republic of Korea.

出版信息

Inflamm Res. 2012 May;61(5):437-44. doi: 10.1007/s00011-011-0430-6. Epub 2012 Jan 12.

Abstract

AIM AND OBJECTIVE

Curcumin, a poly-phenolic compound, possesses diverse pharmacologic activities. However, the barrier protective functions of curcumin or its derivative have not yet been studied. The objective of this study was to investigate the barrier protective activities of curcumin and its derivative (bisdemethoxycurcumin, BDMC) on lipopolysaccharide (LPS) barrier disruption in human umbilical vein endothelial cells (HUVECs) were investigated.

METHODS

The barrier protective effects of curcumin and BDMC such as permeability, expression of cell adhesion molecules, monocytes adhesion and migration toward HUVECs were tested.

RESULTS

Curcumin and BDMC inhibited LPS-induced barrier permeability, monocyte adhesion and migration; inhibitory effects were significantly correlated with inhibitory functions of curcumin and BDMC on LPS-induced cell adhesion molecules (vascular cell adhesion molecules, intracellular cell adhesion molecule, E-selectin). Furthermore, LPS-induced nuclear factor-κB (NF-κB) activation and tumor necrosis factor-α (TNF-α) release from HUVECs were inhibited by curcumin and BDMC. Surprisingly, the barrier protective activities of BDMC were better than those of curcumin, indicating that the methoxy group in curcumin negatively regulated barrier protection function of curcumin.

CONCLUSION

Given these results, curcumin or its derivative, BDMC, showed barrier protective activities and they could be a therapeutic candidates for various systemic inflammatory diseases.

摘要

目的和目标

姜黄素是一种多酚化合物,具有多种药理活性。然而,姜黄素或其衍生物的屏障保护功能尚未得到研究。本研究旨在探讨姜黄素及其衍生物(双去甲氧基姜黄素,BDMC)对人脐静脉内皮细胞(HUVEC)中脂多糖(LPS)屏障破坏的屏障保护作用。

方法

研究了姜黄素和 BDMC 的屏障保护作用,如通透性、细胞黏附分子的表达、单核细胞黏附和向 HUVEC 的迁移。

结果

姜黄素和 BDMC 抑制 LPS 诱导的屏障通透性、单核细胞黏附和迁移;抑制作用与姜黄素和 BDMC 对 LPS 诱导的细胞黏附分子(血管细胞黏附分子、细胞间黏附分子、E-选择素)的抑制作用显著相关。此外,姜黄素和 BDMC 抑制 LPS 诱导的核因子-κB(NF-κB)激活和肿瘤坏死因子-α(TNF-α)从 HUVEC 释放。令人惊讶的是,BDMC 的屏障保护活性优于姜黄素,表明姜黄素中的甲氧基基团负调节姜黄素的屏障保护功能。

结论

鉴于这些结果,姜黄素或其衍生物 BDMC 表现出屏障保护活性,它们可能是各种全身炎症性疾病的治疗候选药物。

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